SAS is characterized by abnormality during sleep and hypoxemia from apnea and hypopnea, followed by systemic inflammation and organ dysfunction like cardiovascular diseases. Systemic inflammation causes the activation of arachidonic acid metabolism, producing prostaglandins (PGs) and leukotrienes (LTs). In addition, significant relationships between PGD2 and PGE2 and sleep, PGF2α and hypertension, PGI2 and thromboxane and platelet aggregation and so on are reported. Therefore, it is hypothesized that many prostanoids affect the pathophysiology of SAS. However, the relationships between prostanoids and clinical outcomes in patients with SAS are unknown. Although CPAP is the major treatment of SAS, the effects of CPAP on prostanoids are not known, either. Thus, the purpose of this study is to evaluate those relationships.